COL3A1 and Myocardial fibrosis: It was predicted by bioinformatics software and experiments in vivo and in vitro that miR.29s could target downregulate the expression of cellular fibrosis-related proteins COLIA1, COLIA2, COL3A1, FBNL, and ELNL and the expression of miR.29s in myocardial infarction tissue was negatively correlated with these proteins, suggesting that miR-29s can inhibit myocardial fibrosis in a myocardial damaged area.